Background: Several prospective studies have revealed that prenatal exposure to polychlorinated biphenyls (PCBs) and other organochlorine compounds (OCs) affect neurodevelopment during infancy. One of the mechanisms by which PCBs might interfere with neurodevelopment is a deficit in thyroid hormone (TH) concentrations.
Objectives: We investigated the potential impact of transplacental exposure to PCBs and hexachlorobenzene (HCB) on TH concentrations in neonates from two remote coastal populations exposed to OCs through the consumption of seafood products.
Methods: Blood samples were collected at birth from the umbilical cord of neonates from Nunavik (n=410) and the Lower North Shore of the St. Lawrence River (n=260) (Québec, Canada) for thyroid parameters [thyroid-stimulating hormone (TSH), free T4 (fT4), total T3 (tT3), and thyroxine-binding globuline (TBG)] and contaminants analyses.
Results: In multivariate models, umbilical cord plasma concentrations of PCB 153, the predominant PCB congener, were not associated with TH and TSH levels in both populations. Prenatal exposure to HCB was positively associated with fT4 levels at birth in both populations (Nunavik, beta=0.12, p=0.04; St. Lawrence, beta=0.19, p<0.01), whereas TBG concentrations were negatively associated with PCB 153 concentrations (beta=-0.13, p=0.05) in the St. Lawrence cohort.
Conclusion: OCs levels were not associated to a reduction in THs in neonates from our two populations. Essential nutrients derived from seafood such as iodine may have prevented the negative effects of OCs on the thyroid economy during fetal development.